Viruses

Research

11 pages, 1783 KiB

Open AccessArticle

Generation and Characterization of Anti-Filovirus Nucleoprotein Monoclonal Antibodies

by Md Niaz Rahim, Min Wang, Tong Wang, Shihua He, Bryan D. Griffin, Darwyn Kobasa, Ruifu Yang, Zongmin Du and Xiangguo Qiu

Viruses 2019, 11(3), 259; https://doi.org/10.3390/v11030259 - 14 Mar 2019

Cited by 6 | Viewed by 3265

Abstract

Filoviruses cause lethal hemorrhagic fever in humans. The filovirus nucleoprotein (NP) is expressed in high abundance in infected cells and is essential for virus replication. To generate anti-filovirus monoclonal antibodies (mAbs) against the NP, mice were immunized with peptides known as B-cell epitopes [...] Read more.

Filoviruses cause lethal hemorrhagic fever in humans. The filovirus nucleoprotein (NP) is expressed in high abundance in infected cells and is essential for virus replication. To generate anti-filovirus monoclonal antibodies (mAbs) against the NP, mice were immunized with peptides known as B-cell epitopes corresponding to different filovirus NPs, and hybridomas were screened using FLAG-tagged filovirus NP constructs. Numerous mAbs were identified, isotyped, and characterized. The anti-NP mAbs demonstrated different ranges of binding affinities to various filovirus NPs. Most of the clones specifically detected both recombinant and wild-type NPs from different filoviruses, including Ebola (EBOV), Sudan (SUDV), Bundibugyo (BDBV), Marburg (MARV), Tai Forest (TAFV), and Reston (RESTV) viruses in western blot analysis. The mAbs were also able to detect native NPs within the cytoplasm of infected cells by immunofluorescence confocal microscopy. Thus, this panel of mAbs represents an important set of tools that may be potentially useful for diagnosing filovirus infection, characterizing virus replication, and detecting NP–host protein interactions. Full article

(This article belongs to the Special Issue CSV2018: The 2nd symposium of the Canadian Society for Virology (CSV))

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13 pages, 2042 KiB

Open AccessArticle

In Vivo Characterization of Avian Influenza A (H5N1) and (H7N9) Viruses Isolated from Canadian Travelers

by Yao Lu, Shelby Landreth, Amit Gaba, Magda Hlasny, Guanqun Liu, Yanyun Huang and Yan Zhou

Viruses 2019, 11(2), 193; https://doi.org/10.3390/v11020193 - 23 Feb 2019

Cited by 11 | Viewed by 5441

Abstract

Highly pathogenic avian influenza (HPAI) H5N1 and low pathogenic avian influenza (LPAI) H7N9 viruses pose a severe threat to public health through zoonotic infection, causing severe respiratory disease in humans. While HPAI H5N1 human infections have typically been reported in Asian countries, avian [...] Read more.

Highly pathogenic avian influenza (HPAI) H5N1 and low pathogenic avian influenza (LPAI) H7N9 viruses pose a severe threat to public health through zoonotic infection, causing severe respiratory disease in humans. While HPAI H5N1 human infections have typically been reported in Asian countries, avian H7N9 human infections have been reported mainly in China. However, Canada reported a case of fatal human infection by the HPAI H5N1 virus in 2014, and two cases of human illness associated with avian H7N9 virus infection in 2015. While the genomes of the causative viruses A/Alberta/01/2014 (H5N1) (AB14 (H5N1)) and A/British Columbia/1/2015 (H7N9) (BC15 (H7N9)) are reported, the isolates had not been evaluated for their pathogenicity in animal models. In this study, we characterized the pathogenicity of AB14 (H5N1) and BC15 (H7N9) and found that both strain isolates are highly lethal in mice. AB14 (H5N1) caused systemic viral infection and erratic proinflammatory cytokine gene expression in different organs. In contrast, BC15 (H7N9) replicated efficiently only in the respiratory tract, and was a potent inducer for proinflammatory cytokine genes in the lungs. Our study provides experimental evidence to complement the specific human case reports and animal models for evaluating vaccine and antiviral candidates against potential influenza pandemics. Full article

(This article belongs to the Special Issue CSV2018: The 2nd symposium of the Canadian Society for Virology (CSV))

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18 pages, 2375 KiB

Open AccessArticle

Characterization of Host and Bacterial Contributions to Lung Barrier Dysfunction Following Co-infection with 2009 Pandemic Influenza and Methicillin Resistant Staphylococcus aureus

by Michaela E. Nickol, Justine Ciric, Shane D. Falcinelli, Daniel S. Chertow and Jason Kindrachuk

Viruses 2019, 11(2), 116; https://doi.org/10.3390/v11020116 - 29 Jan 2019

Cited by 20 | Viewed by 4967

Abstract

Influenza viruses are a threat to global public health resulting in ~500,000 deaths each year. Despite an intensive vaccination program, influenza infections remain a recurrent, yet unsolved public health problem. Secondary bacterial infections frequently complicate influenza infections during seasonal outbreaks and pandemics, resulting [...] Read more.

Influenza viruses are a threat to global public health resulting in ~500,000 deaths each year. Despite an intensive vaccination program, influenza infections remain a recurrent, yet unsolved public health problem. Secondary bacterial infections frequently complicate influenza infections during seasonal outbreaks and pandemics, resulting in increased morbidity and mortality. Staphylococcus aureus, including methicillin-resistant S. aureus (MRSA), is frequently associated with these co-infections, including the 2009 influenza pandemic. Damage to alveolar epithelium is a major contributor to severe influenza-bacterial co-infections and can result in gas exchange abnormalities, fluid leakage, and respiratory insufficiency. These deleterious manifestations likely involve both pathogen- and host-mediated mechanisms. However, there is a paucity of information regarding the mechanisms (pathogen- and/or host-mediated) underlying influenza-bacterial co-infection pathogenesis. To address this, we characterized the contributions of viral-, bacterial-, and host-mediated factors to the altered structure and function of alveolar epithelial cells during co-infection with a focus on the 2009 pandemic influenza (pdm2009) and MRSA. Here, we characterized pdm2009 and MRSA replication kinetics, temporal host kinome responses, modulation of MRSA virulence factors, and disruption of alveolar barrier integrity in response to pdm2009-MRSA co-infection. Our results suggest that alveolar barrier disruption during co-infection is mediated primarily through host response dysregulation, resulting in loss of alveolar barrier integrity. Full article

(This article belongs to the Special Issue CSV2018: The 2nd symposium of the Canadian Society for Virology (CSV))

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11 pages, 2043 KiB

Open AccessCommunication

Class A Scavenger Receptors Are Used by Frog Virus 3 During Its Cellular Entry

by Nguyen T. K. Vo, Matthew Guerreiro, Amulya Yaparla, Leon Grayfer and Stephanie J. DeWitte-Orr

Viruses 2019, 11(2), 93; https://doi.org/10.3390/v11020093 - 23 Jan 2019

Cited by 15 | Viewed by 3831

Abstract

Frog virus 3 (FV3) is the type species of the genus Ranavirus (family Iridoviridae). FV3 and FV3-like viruses are globally distributed infectious agents with the capacity to replicate in three vertebrate classes (teleosts, amphibians, and reptiles). At the cellular level, FV3 and FV3-like [...] Read more.

Frog virus 3 (FV3) is the type species of the genus Ranavirus (family Iridoviridae). FV3 and FV3-like viruses are globally distributed infectious agents with the capacity to replicate in three vertebrate classes (teleosts, amphibians, and reptiles). At the cellular level, FV3 and FV3-like viruses can infect cells from virtually all vertebrate classes. To date, the cellular receptors that are involved in the FV3 entry process are unknown. Class A scavenger receptors (SR-As) are a family of evolutionarily conserved cell-surface receptors that bind a wide range of chemically distinct polyanionic ligands and can function as cellular receptors for other DNA viruses, including vaccinia virus and herpes simplex virus. The present study aimed to determine whether SR-As are involved in FV3 cellular entry. By using well-defined SR-A competitive and non-competitive ligand-blocking assays and absolute qPCR, we demonstrated that the SR-A competitive ligands drastically reduced the quantities of cell-associated viral loads in frog cells. Moreover, inducing the expression of a human SR-AI in an SR-A null cell line significantly increased FV3–cell association. Together, our results indicate that SR-As are utilized by FV3 during the cellular entry process. Full article

(This article belongs to the Special Issue CSV2018: The 2nd symposium of the Canadian Society for Virology (CSV))

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14 pages, 1873 KiB

Open AccessArticle

Genomic-Scale Interaction Involving Complementary Sequences in the Hepatitis C Virus 5′UTR Domain IIa and the RNA-Dependent RNA Polymerase Coding Region Promotes Efficient Virus Replication

by Elodie Rance, Jerome E. Tanner and Caroline Alfieri

Viruses 2019, 11(1), 17; https://doi.org/10.3390/v11010017 - 28 Dec 2018

Cited by 3 | Viewed by 4025

Abstract

The hepatitis C virus (HCV) genome contains structured elements thought to play important regulatory roles in viral RNA translation and replication processes. We used in vitro RNA binding assays to map interactions involving the HCV 5′UTR and distal sequences in NS5B to examine [...] Read more.

The hepatitis C virus (HCV) genome contains structured elements thought to play important regulatory roles in viral RNA translation and replication processes. We used in vitro RNA binding assays to map interactions involving the HCV 5′UTR and distal sequences in NS5B to examine their impact on viral RNA replication. The data revealed that 5′UTR nucleotides (nt) 95–110 in the internal ribosome entry site (IRES) domain IIa and matching nt sequence 8528–8543 located in the RNA-dependent RNA polymerase coding region NS5B, form a high-affinity RNA-RNA complex in vitro. This duplex is composed of both wobble and Watson-Crick base-pairings, with the latter shown to be essential to the formation of the high-affinity duplex. HCV genomic RNA constructs containing mutations in domain IIa nt 95–110 or within the genomic RNA location comprising nt 8528–8543 displayed, on average, 5-fold less intracellular HCV RNA and 6-fold less infectious progeny virus. HCV genomic constructs containing complementary mutations for IRES domain IIa nt 95–110 and NS5B nt 8528–8543 restored intracellular HCV RNA and progeny virus titers to levels obtained for parental virus RNA. We conclude that this long-range duplex interaction between the IRES domain IIa and NS5B nt 8528–8543 is essential for optimal virus replication. Full article

(This article belongs to the Special Issue CSV2018: The 2nd symposium of the Canadian Society for Virology (CSV))

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28 pages, 5702 KiB

Open AccessArticle

Global Interactomics Connect Nuclear Mitotic Apparatus Protein NUMA1 to Influenza Virus Maturation

by Md Niaz Rahim, Ludger Klewes, Ali Zahedi-Amiri, Sabine Mai and Kevin M. Coombs

Viruses 2018, 10(12), 731; https://doi.org/10.3390/v10120731 - 19 Dec 2018

Cited by 5 | Viewed by 6327

Abstract

Influenza A virus (IAV) infections remain a major human health threat. IAV has enormous genetic plasticity and can rapidly escape virus-targeted anti-viral strategies. Thus, there is increasing interest to identify host proteins and processes the virus requires for replication and maturation. The IAV [...] Read more.

Influenza A virus (IAV) infections remain a major human health threat. IAV has enormous genetic plasticity and can rapidly escape virus-targeted anti-viral strategies. Thus, there is increasing interest to identify host proteins and processes the virus requires for replication and maturation. The IAV non-structural protein 1 (NS1) is a critical multifunctional protein that is expressed to high levels in infected cells. Host proteins that interact with NS1 may serve as ideal targets for attenuating IAV replication. We previously developed and characterized broadly cross-reactive anti-NS1 monoclonal antibodies. For the current study, we used these mAbs to co-immunoprecipitate native IAV NS1 and interacting host proteins; 183 proteins were consistently identified in this NS1 interactome study, 124 of which have not been previously reported. RNAi screens identified 11 NS1-interacting host factors as vital for IAV replication. Knocking down one of these, nuclear mitotic apparatus protein 1 (NUMA1), dramatically reduced IAV replication. IAV genomic transcription and translation were not inhibited but transport of viral structural proteins to the cell membrane was hindered during maturation steps in NUMA1 knockdown (KD) cells. Full article

(This article belongs to the Special Issue CSV2018: The 2nd symposium of the Canadian Society for Virology (CSV))

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17 pages, 2772 KiB

Open AccessArticle

Communities of Phytoplankton Viruses across the Transition Zone of the St. Lawrence Estuary

by Myriam Labbé, Frédéric Raymond, Alice Lévesque, Mary Thaler, Vani Mohit, Martyne Audet, Jacques Corbeil and Alexander Culley

Viruses 2018, 10(12), 672; https://doi.org/10.3390/v10120672 - 27 Nov 2018

Cited by 5 | Viewed by 3777

Abstract

The St. Lawrence hydrographic system includes freshwater, brackish, and marine habitats, and is the largest waterway in North America by volume. The food-webs in these habitats are ultimately dependent on phytoplankton. Viral lysis is believed to be responsible for a major part of [...] Read more.

The St. Lawrence hydrographic system includes freshwater, brackish, and marine habitats, and is the largest waterway in North America by volume. The food-webs in these habitats are ultimately dependent on phytoplankton. Viral lysis is believed to be responsible for a major part of phytoplankton mortality. To better understand their role, we characterized the diversity and distribution of two viral taxa infecting phytoplankton: the picornaviruses and phycodnaviruses. Our study focused on the estuary transition zone, which is an important nursery for invertebrates and fishes. Both viral taxa were investigated by PCR amplification of conserved molecular markers and next-generation sequencing at six sites, ranging from freshwater to marine. Our results revealed few shared viral phylotypes between saltwater and freshwater sites. Salinity appeared to be the primary determinant of viral community composition. Moreover, our analysis indicated that the viruses identified in this region of the St. Lawrence diverge from classified viruses and homologous published environmental virotypes. These results suggest that DNA and RNA viruses infecting phytoplankton are likely active in the estuary transition zone, and that this region harbors its own unique viral assemblages. Full article

(This article belongs to the Special Issue CSV2018: The 2nd symposium of the Canadian Society for Virology (CSV))

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13 pages, 2768 KiB

Open AccessArticle

Comprehensive Analysis of Hepatitis B Virus Promoter Region Mutations

by Vanessa Meier-Stephenson, William T. R. Bremner, Chimone S. Dalton, Guido Van Marle, Carla S. Coffin and Trushar R. Patel

Viruses 2018, 10(11), 603; https://doi.org/10.3390/v10110603 - 1 Nov 2018

Cited by 9 | Viewed by 7257

Abstract

Over 250 million people are infected chronically with hepatitis B virus (HBV), the leading cause of liver cancer worldwide. HBV persists, due, in part, to its compact, stable minichromosome, the covalently-closed, circular DNA (cccDNA), which resides in the hepatocytes’ nuclei. Current therapies target [...] Read more.

Over 250 million people are infected chronically with hepatitis B virus (HBV), the leading cause of liver cancer worldwide. HBV persists, due, in part, to its compact, stable minichromosome, the covalently-closed, circular DNA (cccDNA), which resides in the hepatocytes’ nuclei. Current therapies target downstream replication products, however, a true virological cure will require targeting the cccDNA. Finding targets on such a small, compact genome is challenging. For HBV, to remain replication-competent, it needs to maintain nucleotide fidelity in key regions, such as the promoter regions, to ensure that it can continue to utilize the necessary host proteins. HBVdb (HBV database) is a repository of HBV sequences spanning all genotypes (A–H) amplified from clinical samples, and hence implying an extensive collection of replication-competent viruses. Here, we analyzed the HBV sequences from HBVdb using bioinformatics tools to comprehensively assess the HBV core and X promoter regions amongst the nearly 70,000 HBV sequences for highly-conserved nucleotides and variant frequencies. Notably, there is a high degree of nucleotide conservation within specific segments of these promoter regions highlighting their importance in potential host protein-viral interactions and thus the virus’ viability. Such findings may have key implications for designing antivirals to target these areas. Full article

(This article belongs to the Special Issue CSV2018: The 2nd symposium of the Canadian Society for Virology (CSV))

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Graphical abstract

21 pages, 5013 KiB

Open AccessArticle

Identification of Novel Subcellular Localization and Trafficking of HIV-1 Nef Variants from Reference Strains G (F1.93.HH8793) and H (BE.93.VI997)

by Logan R. Van Nynatten, Aaron L. Johnson, Brennan S. Dirk, Emily N. Pawlak, Rajesh Abraham Jacob, S. M. Mansour Haeryfar and Jimmy D. Dikeakos

Viruses 2018, 10(9), 493; https://doi.org/10.3390/v10090493 - 13 Sep 2018

Viewed by 4890

Abstract

The human immunodeficiency virus type 1 (HIV-1) accessory protein Nef, plays an essential role in disease progression and pathogenesis via hijacking the host cellular membrane-trafficking machinery. Interestingly, HIV-1 group-M subtypes display differences in the rate of disease progression. However, few reports investigated how [...] Read more.

The human immunodeficiency virus type 1 (HIV-1) accessory protein Nef, plays an essential role in disease progression and pathogenesis via hijacking the host cellular membrane-trafficking machinery. Interestingly, HIV-1 group-M subtypes display differences in the rate of disease progression. However, few reports investigated how the cellular behaviors and activities of Nef isolates from reference strains may differ between HIV-1 group-M subtypes. Here, we characterize how differing cellular distributions of Nef proteins across group-M subtypes may impact protein function using immunofluorescence microscopy and flow cytometric analysis. We demonstrate that Nef variants isolated from HIV-1 group-M subtypes display differences in expression, with low expressing Nef proteins from reference strains of subtypes G (F1.93.HH8793) and H (BE.93.VI997) also displaying decreased functionality. Additionally, we demonstrate variations in the subcellular distribution and localization of these Nef proteins. Nef from subtype G (F1.93.HH8793) and H (BE.93.VI997) reference strains also failed to colocalize with the trans-Golgi network, and were not differentially localized to cellular markers of multivesicular bodies or lysosomes. Strikingly, our results demonstrate that HIV-1 Nef proteins from reference strains G (F1.93.HH8793) and H (BE.93.VI997) highly colocalize with labeled mitochondrial compartments. Full article

(This article belongs to the Special Issue CSV2018: The 2nd symposium of the Canadian Society for Virology (CSV))

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Review

Jump to: Research, Other

36 pages, 18054 KiB

Open AccessReview

Cat and Mouse: HIV Transcription in Latency, Immune Evasion and Cure/Remission Strategies

by Aurélie Delannoy, Mikaël Poirier and Brendan Bell

Viruses 2019, 11(3), 269; https://doi.org/10.3390/v11030269 - 18 Mar 2019

Cited by 30 | Viewed by 9235

Abstract

There is broad scientific and societal consensus that finding a cure for HIV infection must be pursued. The major barrier to achieving a cure for HIV/AIDS is the capacity of the HIV virus to avoid both immune surveillance and current antiretroviral therapy (ART) [...] Read more.

There is broad scientific and societal consensus that finding a cure for HIV infection must be pursued. The major barrier to achieving a cure for HIV/AIDS is the capacity of the HIV virus to avoid both immune surveillance and current antiretroviral therapy (ART) by rapidly establishing latently infected cell populations, termed latent reservoirs. Here, we provide an overview of the rapidly evolving field of HIV cure/remission research, highlighting recent progress and ongoing challenges in the understanding of HIV reservoirs, the role of HIV transcription in latency and immune evasion. We review the major approaches towards a cure that are currently being explored and further argue that small molecules that inhibit HIV transcription, and therefore uncouple HIV gene expression from signals sent by the host immune response, might be a particularly promising approach to attain a cure or remission. We emphasize that a better understanding of the game of “cat and mouse” between the host immune system and the HIV virus is a crucial knowledge gap to be filled in both cure and vaccine research. Full article

(This article belongs to the Special Issue CSV2018: The 2nd symposium of the Canadian Society for Virology (CSV))

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21 pages, 1485 KiB

Open AccessReview

Back to the Future for Influenza Preimmunity—Looking Back at Influenza Virus History to Infer the Outcome of Future Infections

by Magen Ellen Francis, Morgan Leslie King and Alyson Ann Kelvin

Viruses 2019, 11(2), 122; https://doi.org/10.3390/v11020122 - 30 Jan 2019

Cited by 64 | Viewed by 20870

Abstract

The influenza virus-host interaction is a classic arms race. The recurrent and evolving nature of the influenza virus family allows a single host to be infected several times. Locked in co-evolution, recurrent influenza virus infection elicits continual refinement of the host immune system. [...] Read more.

The influenza virus-host interaction is a classic arms race. The recurrent and evolving nature of the influenza virus family allows a single host to be infected several times. Locked in co-evolution, recurrent influenza virus infection elicits continual refinement of the host immune system. Here we give historical context of circulating influenza viruses to understand how the individual immune history is mirrored by the history of influenza virus circulation. Original Antigenic Sin was first proposed as the negative influence of the host’s first influenza virus infection on the next and Imprinting modernizes Antigenic Sin incorporating both positive and negative outcomes. Building on imprinting, we refer to preimmunity as the continual refinement of the host immune system with each influenza virus infection. We discuss imprinting and the interplay of influenza virus homology, vaccination, and host age establishing preimmunity. We outline host signatures and outcomes of tandem infection according to the sequence of virus and classify these relationships as monosubtypic homologous, monosubtypic heterologous, heterosubtypic, or heterotypic sequential infections. Finally, the preimmunity knowledge gaps are highlighted for future investigation. Understanding the effects of antigenic variable recurrent influenza virus infection on immune refinement will advance vaccination strategies, as well as pandemic preparedness. Full article

(This article belongs to the Special Issue CSV2018: The 2nd symposium of the Canadian Society for Virology (CSV))

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19 pages, 1774 KiB

Open AccessReview

Viruses Teaching Immunology: Role of LCMV Model and Human Viral Infections in Immunological Discoveries

by Mohamed S. Abdel-Hakeem

Viruses 2019, 11(2), 106; https://doi.org/10.3390/v11020106 - 27 Jan 2019

Cited by 18 | Viewed by 8535

Abstract

Virology has played an essential role in deciphering many immunological phenomena, thus shaping our current understanding of the immune system. Animal models of viral infection and human viral infections were both important tools for immunological discoveries. This review discusses two immunological breakthroughs originally [...] Read more.

Virology has played an essential role in deciphering many immunological phenomena, thus shaping our current understanding of the immune system. Animal models of viral infection and human viral infections were both important tools for immunological discoveries. This review discusses two immunological breakthroughs originally identified with the help of the lymphocytic choriomeningitis virus (LCMV) model; immunological restriction by major histocompatibility complex and immunotherapy using checkpoint blockade. In addition, we discuss related discoveries such as development of tetramers, viral escape mutation, and the phenomenon of T-cell exhaustion. Full article

(This article belongs to the Special Issue CSV2018: The 2nd symposium of the Canadian Society for Virology (CSV))

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25 pages, 815 KiB

Open AccessReview

The Incorporation of Host Proteins into the External HIV-1 Envelope

by Jonathan Burnie and Christina Guzzo

Viruses 2019, 11(1), 85; https://doi.org/10.3390/v11010085 - 20 Jan 2019

Cited by 41 | Viewed by 9169

Abstract

The incorporation of biologically active host proteins into HIV-1 is a well-established phenomenon, particularly due to the budding mechanism of viral egress in which viruses acquire their external lipid membrane directly from the host cell. While this mechanism might seemingly imply that host [...] Read more.

The incorporation of biologically active host proteins into HIV-1 is a well-established phenomenon, particularly due to the budding mechanism of viral egress in which viruses acquire their external lipid membrane directly from the host cell. While this mechanism might seemingly imply that host protein incorporation is a passive uptake of all cellular antigens associated with the plasma membrane at the site of budding, this is not the case. Herein, we review the evidence indicating that host protein incorporation can be a selective and conserved process. We discuss how HIV-1 virions displaying host proteins on their surface can exhibit a myriad of altered phenotypes, with notable impacts on infectivity, homing, neutralization, and pathogenesis. This review describes the canonical and emerging methods to detect host protein incorporation, highlights the well-established host proteins that have been identified on HIV-1 virions, and reflects on the role of these incorporated proteins in viral pathogenesis and therapeutic targeting. Despite many advances in HIV treatment and prevention, there remains a global effort to develop increasingly effective anti-HIV therapies. Given the broad range of biologically active host proteins acquired on the surface of HIV-1, additional studies on the mechanisms and impacts of these incorporated host proteins may inform the development of novel treatments and vaccine designs. Full article

(This article belongs to the Special Issue CSV2018: The 2nd symposium of the Canadian Society for Virology (CSV))

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24 pages, 1769 KiB

Open AccessReview

Expanding Repertoire of Plant Positive-Strand RNA Virus Proteases

by Krin S. Mann and Hélène Sanfaçon

Viruses 2019, 11(1), 66; https://doi.org/10.3390/v11010066 - 15 Jan 2019

Cited by 28 | Viewed by 6871

Abstract

Many plant viruses express their proteins through a polyprotein strategy, requiring the acquisition of protease domains to regulate the release of functional mature proteins and/or intermediate polyproteins. Positive-strand RNA viruses constitute the vast majority of plant viruses and they are diverse in their [...] Read more.

Many plant viruses express their proteins through a polyprotein strategy, requiring the acquisition of protease domains to regulate the release of functional mature proteins and/or intermediate polyproteins. Positive-strand RNA viruses constitute the vast majority of plant viruses and they are diverse in their genomic organization and protein expression strategies. Until recently, proteases encoded by positive-strand RNA viruses were described as belonging to two categories: (1) chymotrypsin-like cysteine and serine proteases and (2) papain-like cysteine protease. However, the functional characterization of plant virus cysteine and serine proteases has highlighted their diversity in terms of biological activities, cleavage site specificities, regulatory mechanisms, and three-dimensional structures. The recent discovery of a plant picorna-like virus glutamic protease with possible structural similarities with fungal and bacterial glutamic proteases also revealed new unexpected sources of protease domains. We discuss the variety of plant positive-strand RNA virus protease domains. We also highlight possible evolution scenarios of these viral proteases, including evidence for the exchange of protease domains amongst unrelated viruses. Full article

(This article belongs to the Special Issue CSV2018: The 2nd symposium of the Canadian Society for Virology (CSV))

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13 pages, 6447 KiB

Open AccessReview

Implications of HIV-1 Nef for “Shock and Kill” Strategies to Eliminate Latent Viral Reservoirs

by Xiaomei T. Kuang and Mark A. Brockman

Viruses 2018, 10(12), 677; https://doi.org/10.3390/v10120677 - 30 Nov 2018

Cited by 12 | Viewed by 5751

Abstract

Finding a cure for HIV is challenging because the virus is able to integrate itself into the host cell genome and establish a silent state, called latency, allowing it to evade antiviral drugs and the immune system. Various “shock and kill” strategies are [...] Read more.

Finding a cure for HIV is challenging because the virus is able to integrate itself into the host cell genome and establish a silent state, called latency, allowing it to evade antiviral drugs and the immune system. Various “shock and kill” strategies are being explored in attempts to eliminate latent HIV reservoirs. The goal of these approaches is to reactivate latent viruses (“shock”), thereby exposing them to clearance by viral cytopathic effects or immune-mediated responses (“kill”). To date, there has been limited clinical success using these methods. In this review, we highlight various functions of the HIV accessory protein Nef and discuss their double-edged effects that may contribute to the limited effectiveness of current “shock and kill” methods to eradicate latent HIV reservoirs in treated individuals. Full article

(This article belongs to the Special Issue CSV2018: The 2nd symposium of the Canadian Society for Virology (CSV))

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25 pages, 1235 KiB

Open AccessReview

Synthesis and Translation of Viral mRNA in Reovirus-Infected Cells: Progress and Remaining Questions

by Guy Lemay

Viruses 2018, 10(12), 671; https://doi.org/10.3390/v10120671 - 27 Nov 2018

Cited by 29 | Viewed by 6117

Abstract

At the end of my doctoral studies, in 1988, I published a review article on the major steps of transcription and translation during the mammalian reovirus multiplication cycle, a topic that still fascinates me 30 years later. It is in the nature of [...] Read more.

At the end of my doctoral studies, in 1988, I published a review article on the major steps of transcription and translation during the mammalian reovirus multiplication cycle, a topic that still fascinates me 30 years later. It is in the nature of scientific research to generate further questioning as new knowledge emerges. Our understanding of these fascinating viruses thus remains incomplete but it seemed appropriate at this moment to look back and reflect on our progress and most important questions that still puzzle us. It is also essential of being careful about concepts that seem so well established, but could still be better validated using new approaches. I hope that the few reflections presented here will stimulate discussions and maybe attract new investigators into the field of reovirus research. Many other aspects of the viral multiplication cycle would merit our attention. However, I will essentially limit my discussion to these central aspects of the viral cycle that are transcription of viral genes and their phenotypic expression through the host cell translational machinery. The objective here is not to review every aspect but to put more emphasis on important progress and challenges in the field. Full article

(This article belongs to the Special Issue CSV2018: The 2nd symposium of the Canadian Society for Virology (CSV))

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7 pages, 774 KiB

Open AccessReview

Insight into Influenza: A Virus Cap-Snatching

by Corey De Vlugt, Dorota Sikora and Martin Pelchat

Viruses 2018, 10(11), 641; https://doi.org/10.3390/v10110641 - 16 Nov 2018

Cited by 65 | Viewed by 8646

Abstract

The influenza A virus (IAV) genome consists of eight single-stranded RNA segments. Each segment is associated with a protein complex, with the 3′ and 5′ ends bound to the RNA-dependent RNA polymerase (RdRp) and the remainder associated with the viral nucleoprotein. During transcription [...] Read more.

The influenza A virus (IAV) genome consists of eight single-stranded RNA segments. Each segment is associated with a protein complex, with the 3′ and 5′ ends bound to the RNA-dependent RNA polymerase (RdRp) and the remainder associated with the viral nucleoprotein. During transcription of viral mRNA, this ribonucleoprotein complex steals short, 5′-capped transcripts produced by the cellular DNA dependent RNA polymerase II (RNAPII) and uses them to prime transcription of viral mRNA. Here, we review the current knowledge on the process of IAV cap-snatching and suggest a requirement for RNAPII promoter-proximal pausing for efficient IAV mRNA transcription. Full article

(This article belongs to the Special Issue CSV2018: The 2nd symposium of the Canadian Society for Virology (CSV))

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26 pages, 1329 KiB

Open AccessReview

The Diverse Roles of microRNAs at the Host–Virus Interface

by Annie Bernier and Selena M. Sagan

Viruses 2018, 10(8), 440; https://doi.org/10.3390/v10080440 - 19 Aug 2018

Cited by 83 | Viewed by 9720

Abstract

MicroRNAs (miRNAs) are small, non-coding RNAs that regulate gene expression at the post-transcriptional level. Through this activity, they are implicated in almost every cellular process investigated to date. Hence, it is not surprising that miRNAs play diverse roles in regulation of viral infections [...] Read more.

MicroRNAs (miRNAs) are small, non-coding RNAs that regulate gene expression at the post-transcriptional level. Through this activity, they are implicated in almost every cellular process investigated to date. Hence, it is not surprising that miRNAs play diverse roles in regulation of viral infections and antiviral responses. Diverse families of DNA and RNA viruses have been shown to take advantage of cellular miRNAs or produce virally encoded miRNAs that alter host or viral gene expression. MiRNA-mediated changes in gene expression have been demonstrated to modulate viral replication, antiviral immune responses, viral latency, and pathogenesis. Interestingly, viruses mediate both canonical and non-canonical interactions with miRNAs to downregulate specific targets or to promote viral genome stability, translation, and/or RNA accumulation. In this review, we focus on recent findings elucidating several key mechanisms employed by diverse virus families, with a focus on miRNAs at the host–virus interface during herpesvirus, polyomavirus, retroviruses, pestivirus, and hepacivirus infections. Full article

(This article belongs to the Special Issue CSV2018: The 2nd symposium of the Canadian Society for Virology (CSV))

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Other

Jump to: Research, Review

17 pages, 14066 KiB

Open AccessMeeting Report

CSV2018: The 2nd Symposium of the Canadian Society for Virology

by Nathalie Grandvaux and Craig McCormick

Viruses 2019, 11(1), 79; https://doi.org/10.3390/v11010079 - 18 Jan 2019

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Abstract

The 2nd Symposium of the Canadian Society for Virology (CSV2018) was held in June 2018 in Halifax, Nova Scotia, Canada, as a featured event marking the 200th anniversary of Dalhousie University. CSV2018 attracted 175 attendees from across Canada and around the world, more [...] Read more.

The 2nd Symposium of the Canadian Society for Virology (CSV2018) was held in June 2018 in Halifax, Nova Scotia, Canada, as a featured event marking the 200th anniversary of Dalhousie University. CSV2018 attracted 175 attendees from across Canada and around the world, more than double the number that attended the first CSV symposium two years earlier. CSV2018 provided a forum to discuss a wide range of topics in virology including human, veterinary, plant, and microbial pathogens. Invited keynote speakers included David Kelvin (Dalhousie University and Shantou University Medical College) who provided a historical perspective on influenza on the 100th anniversary of the 1918 pandemic; Sylvain Moineau (Université Laval) who described CRISPR-Cas systems and anti-CRISPR proteins in warfare between bacteriophages and their host microbes; and Kate O’Brien (then from Johns Hopkins University, now relocated to the World Health Organization where she is Director of Immunization, Vaccines and Biologicals), who discussed the underlying viral etiology for pneumonia in the developing world, and the evidence for respiratory syncytial virus (RSV) as a primary cause. Reflecting a strong commitment of Canadian virologists to science communication, CSV2018 featured the launch of Halifax’s first annual Soapbox Science event to enable public engagement with female scientists, and the live-taping of the 499th episode of the This Week in Virology (TWIV) podcast, hosted by Vincent Racaniello (Columbia University) and science writer Alan Dove. TWIV featured interviews of CSV co-founders Nathalie Grandvaux (Université de Montréal) and Craig McCormick (Dalhousie University), who discussed the origins and objectives of the new society; Ryan Noyce (University of Alberta), who discussed technical and ethical considerations of synthetic virology; and Kate O’Brien, who discussed vaccines and global health. Finally, because CSV seeks to provide a better future for the next generation of Canadian virologists, the symposium featured a large number of oral and poster presentations from trainees and closed with the awarding of presentation prizes to trainees, followed by a tour of the Halifax Citadel National Historic Site and an evening of entertainment at the historic Alexander Keith’s Brewery. Full article

(This article belongs to the Special Issue CSV2018: The 2nd symposium of the Canadian Society for Virology (CSV))

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